Portulaca oleracea L. Repairs the Skin Barrier and Alleviates Atopic Dermatitis by Targeting Lipid Metabolism to Regulate the JAK1/STAT3 Signaling Pathway and Downregulate Th2 Inflammatory Cytokines
TL;DR
These findings indicate that POL ameliorates AD by suppressing Th2 inflammation through JAK1/STAT3 signaling, correcting lipid-metabolic disturbances, and restoring skin barrier integrity.
Abstract
Background: Portulaca oleracea L. (POL) has anti-inflammatory and immunomodulatory activities, but its mechanism against atopic dermatitis (AD) remains incompletely understood. Methods: 2,4-dinitrofluorobenzene (DNFB)-induced AD mice were treated orally with POL or dexamethasone for 14 days. We evaluated skin lesions, scratchizng, serum IgE, histopathology, inflammatory cytokines, skin-barrier genes, JAK/STAT phosphorylation, and fecal metabolites. Results: POL alleviated skin lesions and pruritus, reduced serum IgE concentrations, attenuated epidermal hyperplasia and inflammatory-cell and mast-cell infiltration, and restored keratinocyte architecture. It decreased IL-4, IL-13, and IL-31 expression, increased filaggrin and loricrin expression, and inhibited JAK1, STAT1, and STAT3 phosphorylation. Untargeted metabolomics showed that POL mainly regulated unsaturated fatty acid and steroid hormone biosynthesis and restored levels of anti-inflammatory and antiallergic metabolites, including (±)18-HEPE, docosahexaenoyl ethanolamide, and dehydroepiandrosterone. Conclusions: These findings indicate that POL ameliorates AD by suppressing Th2 inflammation through JAK1/STAT3 signaling, correcting lipid-metabolic disturbances, and restoring skin barrier integrity.